细胞外基质金属蛋白酶诱导因子在子痫前期及子痫患者胎盘组织中表达的研究

目的探讨细胞外基质金属蛋白酶诱导因子(EMMPRIN)在子痫前期及子痫患者胎盘组织中的表达及其与子痫前期及子痫发病的关系。方法采用免疫组化链霉菌抗生物素蛋白-过氧化酶连接法和RT-PCR技术检测不同孕周的44例子痫前期(重度)孕妇(子痫前期组)、38例子痫孕妇(子痫组)和49例正常孕妇(正常妊娠组)胎盘组织中EMMPRIN蛋白及mRNA的表达。结果(1)EMMPRIN蛋白阳性表达：子痫前期组EMMPRIN蛋白表达中度阳性率为18%(8/44),强阳性率为9%(4/44);子痫组EMMPRIN蛋白中度阳性率为21%(8/38),强阳性率为13%(5/38),两组分别比较,差异均无统计学意义(P＞0．05)。正常妊娠组EMMPRIN蛋白表达中度阳性率为12%(6/49),强阳性率为82%(40/49),与子痫前期组及子痫组比较,差异均有统计学意义(P＜0．001)。(2) EMMPRIN mRNA表达：子痫前期组孕晚期(37～40周)EMMPRIN mRNA为0．342±0．002,子痫组为0．344±0．023,两组比较,差异均无统计学意义(P＞0．05)。正常妊娠组孕晚期(37～40周) EMMPRIN mRNA为0．872±0．094,分别与子痫前期组及子痫组比较,差异均有统计学意义(P＜0．001)。结论子痫前期及子痫患者胎盘组织中EMMPRIN表达水平下降是子痫前期及子痫发病的重要原因;EMMPRIN可作为子痫前期及子痫发病的一个预测指标。     

基质金属蛋白酶3及其抑制剂3在子痫前期患者胎盘中的表达

目的:通过检测子痫前期患者胎盘组织中基质金属蛋白酶3(MMP-3)及其抑制剂3(TIMP-3)的表达,以探讨两者的关系及其在子痫前期发病中的作用。方法:收集34例子痫前期患者(子痫前期组)及32例正常晚期妊娠妇女(正常对照组)的胎盘组织,用免疫组化法检测MMP-3及TIMP-3在胎盘组织中的表达。同时进行HE染色,选取5个高倍视野,计数绒毛血管数。结果:①MMP-3和TIMP-3在胎盘组织的蜕膜细胞和绒毛滋养细胞均有表达。②子痫前期组胎盘蜕膜细胞和绒毛滋养细胞中MMP-3的表达均显著低于对照组(P<0.01)。TIMP-3在子痫前期组胎盘蜕膜细胞和绒毛滋养细胞中的表达量均显著高于对照组(P<0.01)。③子痫前期组胎盘绒毛血管密度明显低于对照组(P<0.01)。结论:子痫前期患者胎盘中MMP-3与TIMP-3的表达情况与正常晚期妊娠妇女存在差异,提示妊娠妇女胎盘组织中MMP-3和TIMP-3的表达水平变化可能与子痫前期的发生、发展相关。     

基质金属蛋白酶与子痫前期发病关系的研究

目的 探讨基质金属蛋白酶(MMP)2、9在子痫前期患者胎盘绒毛中的表达及其与子痫前期发病的关系.方法 采用免疫组化链霉亲和素-生物素-过氧化物酶复合物(SABC)法检测20例子痫前期患者(病例组)和20例正常孕妇(对照组)胎盘绒毛MMP-2、9的表达,实时荧光定量RT-PCR检测两组孕妇胎盘绒毛MMP-2、9 mRNA的表达水平.因提取后的mRNA部分降解,用于RT-PCR检测的胎盘绒毛病例组13份,对照组10份.采用2-△△Ct相对定量表示PCR结果.结果 对照组孕妇胎盘绒毛MMP-2、9的染色强度均高于病例组,两组比较,差异有统计学意义(P＜0.05);对照组胎盘绒毛MMP-2 mRNA的平均表达水平为7.6±2.8,病例组胎盘绒毛MMP-2 mRNA的平均表达水平为5.6±1.5,两组比较,差异有统计学意义(P＜0.05).对照组胎盘绒毛MMP-9 mRNA的平均表达水平为2.2±2.6,高于病例组的-0.9±2.0,两组比较,差异也有统计学意义(P＜0.05).对照组胎盘绒毛MMP-2的平均表达水平高于MMP-9,两者比较,差异有统计学意义(P＜0.05).结论 MMP-2、9表达降低导致的滋养细胞侵袭能力的下降,可能与子痫前期的发病相关.     

子痫前期患者滋养细胞中KiSS-1基因及基质金属蛋白酶9表达的临床意义

目的探讨胎盘滋养细胞中KiSS-1基因及基质金属蛋白酶(MMP)9在子痫前期发病中的作用及其与新生儿预后的相关性。方法采用RT-PCR和western blot(蛋白印迹法)检测40例子痫前期患者(其中轻度15例、重度25例,子痫前期组)和20例正常足月正常妊娠妇女(正常妊娠组)胎盘滋养细胞中KiSS-1mRNA和MMP-9mRNA及其蛋白的表达,并与其临床症状及其新生儿围产结局进行相关性分析。结果(1)子痫前期组滋养细胞中KiSS-1mRNA及其蛋白表达水平分别为1.73±0.24和(78.4±8.0)μg/100μg总蛋白,其中轻度患者为1.50±0.15和(72.4±6.9)μg/100μg总蛋白,重度患者为1.87±0.20和(83.5±3.6)μg/100μg总蛋白;均显著高于正常妊娠组的1.24±0.25和(63.4±2.7)μg/100μg总蛋白(P<0.01)。(2)子痫前期组MMP-9mRNA及其蛋白表达水平分别为0.09±0.06和(9.6±4.3)μg/100μg总蛋白,其中轻度患者为0.11±0.08和(10.0±3.2)μg/100μg总蛋白,重度患者为0.07±0.05和(7.8±2.0)μg/100μg总蛋白;均显著低于正常妊娠组的0.17±0.10和(17.9±7.3)μg/100μg总蛋白(P<0.01)。(3)子痫前期组KiSS-1mRNA及其蛋白表达水平与中心动脉压(MAP)和24h尿蛋白定量呈正相关,r分别为0.610(P=0.023)、0.713(P=0.011)和0.397(P=0.003)、0.638(P=0.002);与有、无眼底动脉痉挛呈显著正相关,r分别为0.499(P=0.000)和0.511(P=0.000)。子痫前期组MMP-9mRNA及其蛋白表达水平则与MAP、24h尿蛋白定量及有、无眼底动脉痉挛呈显著负相关,r分别为0.561(P=0.042)、0.571(P=0.022)、0.275(P=0.039)、0.375(P=0.048)、0.346(P=0.001)、0.543(P=0.000)。(4)子痫前期组MMP-9mRNA及其蛋白表达水平与新生儿体重呈显著正相关,r分别为0.651(P=0.000)和0.544(P=0.004);KiSS-1mRNA及其蛋白表达水平与其呈显著负相关,r分别为0.759(P=0.000)和0.865(P=0.000)。(5)随着新生儿窒息程度加重,MMP-9mRNA及其蛋白表达水平呈降低趋势,KiSS-1mRNA及其蛋白表达水平呈升高趋势(P均<0.05)。结论MMP-9和KiSS-1表达失衡在子痫前期发病中起重要作用,且与新生儿预后密切相关。     

基质金属蛋白酶9在妊娠期高血压疾病中的表达

目的:探讨基质金属蛋白酶9(MMP-9)在妊娠期高血压疾病患者中的表达。方法:ELISA法和免疫组织化学法研究妊娠期高血压疾病患者和正常孕妇血清及胎盘中MMP-9的表达。结果:妊娠期高血压疾病患者血清中MMP-9水平与正常孕妇的差异无统计学意义(P>0.05)。妊娠期高血压疾病患者胎盘MMP-9的表达水平显著低于正常孕妇,差异有统计学意义(P<0.05)。结论:胎盘MMP-9表达下降可能与妊娠期高血压疾病的发生发展相关。     

TGF-β和IGF表达异常与滋养层相关疾病关系的研究

目的:探讨转化生长因子(TGF-β)和胰岛素样生长因子(IGF)等与滋养层侵入调节密切相关的细胞因子在胎盘绒毛组织中的表达,及与葡萄胎、先兆子痫等滋养层细胞相关妊娠疾病病理机制的关系。方法:采用半定量逆转录多聚酶链反应(RT-PCR)检测方法,分别以正常早孕绒毛和正常足月(自然分娩或剖宫产)胎盘绒毛组织为对照,观察葡萄胎组织与先兆子痫足月胎盘绒毛组织中TGF-β和IGF的表达。结果:5种胎盘绒毛组织中均可检测到IGF-I mRNA的表达,且先兆子痫足月胎盘绒毛组织中IGF-I的表达量明显低于正常足月胎盘绒毛组织,而葡萄胎组织中IGF-I的表达略高于正常早孕绒毛。在3种足月胎盘绒毛组织中可检测到IGF-ⅡmRNA的表达,但相互之间无明显差异。葡萄胎组织中IGF-Ⅱ的表达低于早孕绒毛。5种胎盘绒毛组织中均有TGF-β3的表达,而TGF-β1和TGF-β2的表达并未检测到。在表达量上,葡萄胎组织中TGF-β3的表达明显高于正常早孕绒毛组织,先兆子痫胎盘绒毛组织中TGF-β3的表达强于足月自然分娩的正常胎盘绒毛组织,而剖宫产胎盘绒毛组织中,TGF-β3的表达亦相对较强。结论:TGF-β3和IGF-I在胎盘绒毛组织中的表达变化,可能和葡萄胎、先兆子痫等与滋养层密切相关的妊娠疾病的发生有关。     

基质金属蛋白酶与胎盘发育

基质金属蛋白酶 (m atrix m etalloproteinases,MMPs)是一族具有降解细胞外基质 (ECM)成分特性的锌依赖性内切肽酶。在组织塑型过程中影响着 ECM的代谢、新生血管的形成等过程 ,参与创伤的修复 ,并在肿瘤的发生和转移过程中起着重要作用。 MMPs在胚胎植入和胎盘发育过程中 ,其表达在空间和时间上受到的精密调控 ,对妊娠发生和维持正常的妊娠状态具有重要意义。一、基质金属蛋白酶的生物学特征自 196 2年发现间质胶原酶 MMP- 1与蝌蚪尾巴的吸收有关 ,至今人们已经发现至少 17种 MMPs[1 ]。它们具有以下特性 :(1)一级结构中含有一个半…     

子宫内膜癌中基质金属蛋白酶及其组织抑制因子的表达与临床意义

目的研究基质金属蛋白酶(MMPs)- 2、9及其组织抑制因子(TIMPs)- 1、2在子宫内膜癌中的表达并探讨其与子宫内膜癌浸润转移的关系.方法应用免疫组织化学方法对121例子宫内膜癌组织及20例子宫脱垂妇女子宫内膜组织中MMP2、MMP9、TIMP1、TIMP2蛋白进行检测.结果MMP2、MMP9、TIMP1、TIMP2蛋白主要分布在内膜癌细胞中,在间质中也有少量表达.MMP2、MMP9、TIMP1、TIMP2在内膜癌细胞表达的阳性率均高于正常对照组.MMP2、MMP9蛋白的表达,在内膜癌细胞病理分级为G2、G3中,强阳性率高于G1者(P＜0.05);有肌层浸润内膜癌的强阳性率明显高于无肌层浸润者(P＜0.05);有淋巴转移者高于无淋巴转移者(P＜0.05);手术病理分期Ⅲ、Ⅳ期的强阳性率明显高于Ⅰ、Ⅱ期者(P＜0.05).TIMP1蛋白的表达在不同病理分级中差异无显著性(P＞0.05),在深肌层浸润内膜癌中阳性率低于浅肌层浸润(P＜0.05);有淋巴转移者的阳性率低于无淋巴转移者(P＜0.005),手术病理分期为Ⅲ、Ⅳ者阳性率低于Ⅰ期者(P＜0.05);TIMP2蛋白在不同病理分级、肌层浸润、淋巴转移和手术病理分期中的表达率比较,差异均无显著性(P＞0.05).结论MMP2、MMP9蛋白在内膜癌中的表达随病理分级而升高,随肌层浸润程度的加深及有淋巴转移而增加,TIMP1表达随肌层浸润程度的加深及有淋巴转移而下降.     

解整合素金属蛋白酶10在重度子痫前期胎盘中的表达及其意义

目的通过对孕妇胎盘组织中解整合素金属蛋白酶10（a disintegrin and metalloproteinase 10,ADAM10）的检测,探讨ADAM10与子痫前期发病的关系。方法选择2009年9月至2012年3月在北京大学人民医院产科住院分娩的30例重度子痫前期（子痫前期组）和30例正常孕妇（正常妊娠组）,采用反转录聚合酶链反应（RT—PCR）方法检测两组孕妇胎盘组织中ADAM10 mRNA的表达,并采用免疫组化二步法和蛋白质印迹法（Western Blot）检测胎盘组织中ADAM10蛋白的表达。结果ADAM10表达于胎盘组织的细胞滋养细胞和合体滋养细胞的细胞浆和细胞核中。子痫前期组中ADAM10 mRNA及蛋白的表达均明显高于正常妊娠组（P〈0．05）。结论重度子痫前期胎盘组织中ADAM10的过度表达可能与子痫前期的发生和发展有关。     

基质金属蛋白酶与早产的关系

由于早产机制未完全阐明,故早产发生率及早产儿发病率和死亡率一直无明显下降,感染和胎膜早破是早产的主要原因,近来研究认为感染和胎膜早破引起的早产和妊娠妇女体内基质金属蛋白酶(MMPs)的含量变化有关,这两种情况引起的早产发生前,母体血、尿及羊水中的MMPs含量将升高,从而降解妊娠组织的细胞外基质(ECM),引起胎膜破裂及宫颈成熟扩张,而导致早产,且测定妊娠妇女体内MMPs的含量变化可进行早产预测以及应用其抑制剂在动物实验中可降低早产的发生率.     

Differential expression of human placental PAPP-A2 over gestation and in preeclampsia

IntroductionPregnancy Associated Plasma Protein A2 (PAPP-A2) is a pregnancy related insulin-like growth factor binding protein-5 (IGFBP-5) protease, known to be elevated in preeclampsia. As the insulin-like growth factors are important in human implantation and placentation, we sought to determine the expression pattern of PAPP-A2 over human gestation in normal and preeclamptic pregnancies to evaluate its role in placental development and the pathogenesis of preeclampsia.MethodsPlacental basal plate and chorionic villi samples, maternal and fetal cord blood sera were obtained from preeclamptic and control pregnancies. Formalin-fixed tissue sections from across gestation were stained for cytokeratin-7, HLA-G, and PAPP-A2. PAPP-A2 immunoblot analysis was also performed on protein lysates and sera.ResultsPAPP-A2 expression is predominately expressed by differentiated trophoblasts and fetal endothelium. Chorionic villi show strong expression in the first trimester, followed by a progressive decrease in the second trimester, which returns in the third trimester. PAPP-A2 expression is not impacted by labor. PAPP-A2 is increased in the basal plate, chorionic villi and maternal sera in preeclampsia compared to controls, but is not detectable in cord blood.DiscussionPAPP-A2 is differentially expressed in different trophoblast populations and shows strong down regulation in the mid second trimester in chorionic villous samples. Both maternal sera and placental tissue from pregnancies complicated by preeclampsia show increased levels of PAPP-A2. PAPP-A2 levels are not altered by labor. Additionally, PAPP-A2 cannot be detected in cord blood demonstrating that the alterations in maternal and placental PAPP-A2 are not recapitulated in the fetal circulation.     

Difference in the expression of alpha 7 nicotinic receptors in the placenta in normal versus severe preeclampsia pregnancies

OBJECTIVE: The prevalence of preeclampsia is low in smokers, suggesting a possible role of nicotinic receptor in the pathophysiology of the disease. Alpha 7 nicotinic acetylcholine receptor (alpha7 nAChR) was recently found in non-neuronal tissue with various mediating functions. Therefore, we investigated the difference in the placental expression of the alpha7 nAChR in normal versus severe preeclampsia placentas. STUDY DESIGN: Central portions of placenta were obtained from 9 severe preeclampsia women and 11 gestational-age-matched normal pregnant women delivered between the gestational ages of 33 and 40 weeks following elective or emergency cesarean section. RT-PCR, western blotting, and immunohistochemical staining were performed to evaluate the alpha7 nAChR expression difference. RESULTS: In all the placentas, the alpha7 nAChR was expressed in endothelial cells, vascular smooth muscle cells, and stromal cells, but not in trophoblasts. The vascular staining was more intense in the severe preeclampsia placenta (p=0.02). Although the gene expression did not differ between the two groups, protein expression was greater in 7 of 9 placenta samples from the severe preeclampsia group. CONCLUSION: Placental expression of alpha7 nAChR differs between normal and severe preeclampsia placentas, suggesting that it may be involved in the pathogenesis of preeclampsia.     

Association between first-trimester placental volume and birth weight

Objective

To estimate the correlation between first-trimester placental volume, birth weight, small-for-gestational-age (SGA), and preeclampsia.

Methods

A prospective study of women with singleton pregnancy at 11–13 weeks of gestation was conducted. First-trimester placental volume was measured using three-dimensional ultrasound and reported as multiple of median (MoM) for gestational age. Participants were followed until delivery where birth weight, placental weight, and occurrence of preeclampsia were collected. Non-parametric analyses were performed.

Results

We reached a complete follow-up for 543 eligible women. First-trimester placental volume was significantly correlated with birth weight (correlation coefficient: 0.18; p < 0.0001) and placental weight (cc: 0.22; p < 0.0001) adjusted for gestational age. First-trimester placental volume was smaller in women who delivered SGA neonates (median MoM: 0.79; interquartile range: 0.62–1.00; p < 0.001) and greater in women who delivered large-for-gestational-age neonates (median MoM: 1.13; 0.95–1.49; p < 0.001) when compared to women with neonates between the 10th and 90th percentile (median MoM: 1.00; 0.81–1.25). First-trimester placental volume was not associated with the risk of preeclampsia (cc: 0.01; p = 0.87).

Conclusion

First-trimester placental volume is strongly associated with fetal and placental growth. However, we did not observe a correlation between placental volume and the risk of preeclampsia.     

Differential expression and the anti-apoptotic effect of human placental neurotrophins and their receptors

Neurotrophin (NT) is important in the survival, maintenance and differentiation of neuronal tissue, and functions in follicle maturation, tumor growth, angiogenesis and immunomodulation; however, the expression of NT and its receptors (NTR) in human placenta and their influence on fetal growth are unclear. Here we investigated the correlation of NT and NTR in human placenta with uterine environment and fetal growth. TrkB, a NTR, mRNA was expressed on decidual and villous tissue and increased with gestational age, localizing in the trophoblast layer and endothelium by immunohistochemistry. Villous TrkB mRNA was significantly increased in preeclampsia (PE) than in controls and was higher in the normotensive small for gestational age (SGA) placenta, although it was not significant. It was also significantly increased in the small twin of discordant twin pregnancies. Brain-derived neurotrophic factor (BDNF), the main ligand of TrkB, was expressed in membranous chorion and villous tissue and was significantly higher in maternal plasma in normotensive SGA and PE than in controls. TrkB mRNA expression was up-regulated on cultured villous tissue explants and on JEG-3, a choriocarcinoma cell line, by H₂O₂ treatment. BDNF decreased apoptotic cells in H₂O₂-treated JEG-3, indicating that BDNF/TrkB signaling had anti-apoptotic effects against oxidative stress in JEG-3, suggesting a protective role of BDNF/TrkB in human villous tissue under unfavorable conditions in utero.     

子痫前期患者胎盘组织中松弛素受体的表达

目的 探讨子痫前期患者胎盘组织中松弛素受体LGR7表达与子痫前期发病的关系.方法 应用链霉菌抗生物素蛋白-过氧化物酶连接法和RT-PCR技术检测20例正常孕妇(正常组)及26例重度子痫前期孕妇(子痫前期组)胎盘组织中松弛素受体LGR7蛋白及mRNA的表达.结果 (1)两组孕妇的胎盘组织中均有松弛素受体LGR7表达,主要定位于胎盘绒毛滋养细胞的细胞膜上,在细胞滋养细胞、合体滋养细胞中都有较高的表达水平.(2)正常组胎盘组织中松弛素受体LGR7蛋白的表达水平为0.912±0.003,子痫前期组为0.625±0.037,两组比较,差异有统计学意义(P＜0.01).(3)正常组胎盘组织中松弛素受体LGR7 mRNA表达水平为0.776±0.021,子痫前期组为0.393±0.075,两组比较,差异有统计学意义(P＜0.01).结论 子痫前期患者胎盘组织中松弛素受体表达水平下降,可能与子痫前期的发病有关.     

正常及妊娠高血压综合征孕妇胎盘组织中去甲肾上腺素和多巴胺的研究

目的　通过对正常孕妇及妊娠高血压综合征 (妊高征 )孕妇胎盘组织中去甲肾上腺素(NE)及多巴胺 (DA)的定位及定量测定 ,探讨其与妊高征发病的关系。方法　应用免疫组织化学 (免疫组化 )链霉素抗生物素 -过氧化物酶法 ,对 31例正常早、中、晚孕妇女 (正常孕妇组 ) ,及 38例轻、中、重度妊高征孕妇 (妊高征孕妇组 )的胎盘组织进行NE和DA定位 ;并应用电子计算机图像分析系统进行定量 ,其结果以灰度值倒数表示。结果　 (1)两组孕妇胎盘组织NE及DA免疫组化定位 :正常孕妇组中 ,早期孕妇的胚胎绒毛滋养细胞NE及DA免疫反应呈现强阳性 ,呈深棕色 ,定位于细胞滋养细胞的细胞膜及细胞浆中 ;中、晚期孕妇胎盘组织NE及DA免疫反应表现为阳性 ,呈棕色 ,或弱阳性呈浅棕色 ,定位于合体滋养细胞的细胞膜及细胞浆 ,以及毛细血管内皮。妊高征孕妇组的胎盘组织NE、DA定位与正常孕妇组中的晚期孕妇相同。 (2 )两组孕妇胎盘组织NE及DA免疫组化定量 (灰度倒数值 ) :正常孕妇组NE由孕早期的 1 5 95± 0 0 18降至中、晚期的 1 4 88± 0 0 19和 1 4 19± 0 0 14 (P<0 0 1) ;DA由孕早期的 1 5 5 2± 0 0 6 7,降至中、晚期的 1 36 9± 0 0 5 1和 1 30 2± 0 0 13(P <0 0 1)。妊高征孕妇组妊高征轻、中、重度的DA ,依次为 1 37     

子痫前期患者血浆中sTRAIL、胎盘组织TRAIL及TRAIL受体的变化及意义

目的:研究子痫前期(PE)患者血浆s TRAIL及胎盘滋养细胞上TRAIL/TRAIL-Rs的变化及其与PE发病的关系。方法:选取56例PE患者为研究对象,其中符合重度PE诊断标准者31例(研究组1),未及重度PE 25例(研究组2)。选取同期正常妊娠妇女为对照组,其中28~36周30例(对照组1)、36~(+1)~38周30例(对照组2),因胎膜早破、早产等于28~36周分娩者27例(对照组3),36~(+1)~38周分娩者30例(对照组4)。研究组孕妇留取静脉血及胎盘组织,对照组1、2留取静脉血,对照组3、4留取胎盘组织。ELISA法检测血浆中TRAIL含量,免疫组化法检测胎盘组织中TRAIL和TRAIL-Rs(DR4、DR5、DcR1、DcR2)含量。结果:研究组血浆中sTRAIL含量明显低于对照组(研究组1 vs对照组1,P0.001;研究组2 vs对照组2,P0.005);随着病情加重,s TRAIL含量明显下降(P0.05)。研究组胎盘组织中TRAIL表达明显减少,随着病情加重而加重。研究组中死亡受体DR4、DR5的含量明显高于对照组,而诱骗受体DcR1、DcR2含量明显低于对照组。PE重度组中DR4、DR5含量高于轻度组(P0.05),DcR1和DcR2含量则无显著差异。结论:PE患者血浆中sTRAIL及胎盘组织中TRAIL/TRAIL-Rs含量发生了明显变化,TRAIL/TRAIL-Rs的不平衡性参与了PE的病理过程。     

人类白细胞相关抗原-G及其各亚型mRNA在正常妊娠及重度子前期患者胎盘组织中的表达

目的研究人类白细胞相关抗原-G(HLA-G)及其各个亚型mRNA在正常妊娠及重度子前期患者胎盘组织中的表达。方法选取2005-01-2005-06第四军医大学唐都医院10例重度子前期患者(研究组)及10例正常妊娠胎盘组织(对照组),应用荧光定量RT-PCR比较两组间HLA-G及其各个亚型mRNA(HLA-G1、G2、G3、G4、G5、G6)的表达。结果与对照组相比,重度子前期患者胎盘组织中总HLA-GmRNA显著降低,以HLA-G1、HLA-G3降低为主,差异有统计学意义(P<0.05)。结论HLA-G1与HLA-G3在胎盘组织中的低表达可能与妊娠期高血压疾病的发病和病理生理过程有关。     

血清、脐血中MPO水平变化及胎盘组织MPO mRNA表达与子痫前期发病的关系

目的:研究重度子痫前期(PE)患者血清MPO及胎盘组织中MPO mRNA表达水平变化与PE发病的关系,探讨糖脂代谢异常及氧化应激在PE病理生理机制中的可能作用。方法:选取60例重度PE孕妇,按发病时孕周不同分为早发型PE组(孕周34周)和晚发型PE组(孕周≥34周)各30例。另选取同期健康晚期妊娠孕妇60例,分为对照1组(孕周34周)和对照2组(孕周≥34周)各30例。采用实时荧光定量PCR技术检测胎盘组织中MPO mRNA表达水平;ELISA法检测血清MPO水平。检测患者血压、血脂、血糖、胰岛素水平等指标,进行相关性分析。结果:PE组的血清MPO水平高于对照组(P0.05),且早发型高于晚发型PE组(P0.05);但对照组间比较无差异(P0.05)。PE组的血清TC、TG、LDL、FINS、HOMA-IR分别高于对照组(P0.05),HDL水平低于对照组(P0.05);但PE组间比较及对照组间比较,均无差异(P0.05)。PE组的脐血MPO水平、胎盘组织中MPO mRNA表达水平均高于对照2组(P0.05),且早发型高于晚发型组(P0.05)。PE组的血清MPO水平与TG、HoMA-IR、FINS、胎盘组织MPO mRNA表达水平均呈正相关(r=0.557、0.615;0.694、0.511;0.766、0.717;0.696、0.695),与血HDL呈负相关(r=-0.697,-0.576);对照2组则无相关性。结论:MPO可能参与了PE的病理生理过程。胎盘组织中MPO mRNA表达水平升高可能是血清MPO水平升高的重要原因。PE患者血脂代谢异常及胰岛素抵抗增加与血清MPO水平升高有关,它们可能参与了血清MPO水平升高后促发PE的氧化应激的病理生理过程。